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Individuals with severe depression are often stripped of the capacity to engage with the world in rewarding ways. The presence of this hallmark symptom of depression - anhedonia, or diminished reward sensitivity (RS) - is associated with poorer treatment response and elevated risk for suicide. Despite clinical evidence that low RS is a debilitating feature of major depressive disorder (MDD), little is known about how RS relates to variation in neural reward processing, particularly in early life. Given that affective disorders commonly appear in adolescence, characterizing trait-brain relations during development has critical implications for understanding disease development. The present study tested how variation in RS and negative affect (NA), two core MDD risk traits, uniquely and interactively predict variation in brain reward function in a high-risk (i.e., low income, minority) youth sample. Neural responses during reward processing were examined using a functional magnetic resonance imaging (fMRI) reward task. RS was derived from the Behavioral Inhibition and Activation Scales (BIS/BAS), and NA was computed using the Children's Depression Inventory (CDI) and the Screen for Child Anxiety Related Emotional Disorders (SCR). RS and NA were uncorrelated, validating the unique distribution of these phenotypes across individuals. Variation in RS and NA were associated with unique patterns of reward-related neural activity in the dorsolateral prefrontal cortex, striatum, and medial prefrontal cortex. An interaction between RS and NA was observed in the thalamus, a primary region of reward circuitry. The addition of low RS to high NA was associated with further blunting of neural responses to reward, particularly in the thalamus. Our results underscore the importance of assessing critical MDD risk traits simultaneously.

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